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Çocuklarda Covid 19 İlişkili Multisistem İnflamatuar Sendrom Patofizyolojisi

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dc.creator AKKUZU, Emine; Isparta City Hospital
dc.date 2021-06-05T00:00:00Z
dc.date.accessioned 2021-12-03T11:46:55Z
dc.date.available 2021-12-03T11:46:55Z
dc.identifier https://dergipark.org.tr/tr/pub/sdutfd/issue/62643/906833
dc.identifier 10.17343/sdutfd.906833
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/94147
dc.description Koronavirüs hastalığı 2019 (COVID-19) salgını ilk kez Asya'da rapor edildiğinde ve ardından tüm dünyaya yayıldığında, ilk bulgular enfeksiyonun çocuklarda daha hafif semptomlarla görüldüğü şeklindeydi. Ancak Nisan 2020 ortalarında önce İngiltere, ardından İtalya, İspanya, Amerika olmak üzere bir çok ülkeden çoklu organ yetmezliği bulgularıyla başvuran hastalar rapor edildi ve yeni bir hiperinflamatuar sendrom olan çocuklarda multisistem inflamatuar sendrom (MIS-C) tanımlandı. MIS-C’nin erişkinlerdeki şiddetli akut respiratuvar sendromu koronavirüsü 2 (SARS-CoV-2) piklerinden 4-6 hafta sonra görülme sıklığı artması nedeniyle bir enfeksiyon sonrası süreç olduğu düşünülmektedir. MIS-C Kawasaki hastalığı, sitokin salınım sendromu, makrofaj aktivasyon sendromu ile benzerlikleri olsa da ayrı bir immün fenotipe sahiptir. MIS-C patofizyolojisi ve neden bazı çocuklarda gelişip diğerlerinde gelişmediği net bilinmemektedir. Çocuklarda genellikle asemptomatik veya hafif semptomlarla geçen erken enfeksiyon, makrofaj aktivasyonuna ve ardından yardımcı T hücrelerin uyarılmasına neden olur. Bunun sonucunda tümör nekrozis faktör (TNF), interlökin (IL)-6, IL-1β, IL-4, IL-23, IL-18, IL-12 ve interferon (IFN) gibi sitokinlerin salınımına/fırtınasına, makrofajların, nötrofillerin ve monositlerin uyarılmasına neden olur. MIS-C patogenezini anlamak ve COVID-19 pandemisi yeni piklerle devam ederken tedavisine ve önlenmesine rehberlik etmek için daha fazla araştırma yapılması zorunludur.
dc.description When the coronavirus disease 2019 (COVID-19) outbreak was first reported in Asia and then spread worldwide, the initial findings showed that the infection was milder in children. However, in mid-April 2020, patients from many countries, first in England, then Italy, Spain, and United States of America, were reported with multiple organ failure symptoms, and multisystem inflammatory syndrome (MIS-C) was identified in children as a new hyperinflammatory syndrome. MIS-C is thought to be a post-infection process due to its increased incidence 4-6 weeks after the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) peaks in adults. Although it has similarities with Kawasaki disease, cytokine release syndrome and macrophage activation syndrome have a separate immune phenotype. The pathophysiology of MIS-C and why it develops in some children and not in others is not clear. Early infection, usually asymptomatic or with mild symptoms in children, causes macrophage activation followed by stimulation of helper T cells. This causes the release of cytokines such as tumor necrosis factor (TNF), interleukin (IL)-6, IL-1β, IL-4, IL-23, IL-18, IL-12, and interferon (IFN) and stimulation of macrophages, neutrophils, and monocytes. Further research is imperative to understand the pathogenesis of MIS-C and to guide its treatment and prevention as the COVID-19 pandemic continues with new peaks.
dc.format application/pdf
dc.language tr
dc.publisher Süleyman Demirel Üniversitesi
dc.publisher Süleyman Demirel University
dc.relation https://dergipark.org.tr/tr/download/article-file/1674087
dc.source Volume: COVID-19 Özel Sayı, Issue: 1 93-96 en-US
dc.source 1300-7416
dc.source 2602-2109
dc.source SDÜ Tıp Fakültesi Dergisi
dc.subject MIS-C,Multisistem inflamatuar sendrom,çocuklar,SARS-CoV-2,COVID-19,patofizyoloji,immün yanıt,interlökin
dc.subject MIS-C,Multisystem inflammatory syndrome,children,SARS-CoV-2,COVID-19,pathogenesis,immune response,interleukin
dc.title Çocuklarda Covid 19 İlişkili Multisistem İnflamatuar Sendrom Patofizyolojisi tr-TR
dc.title Pathophysıology of Covıd 19 Related Multisystem Inflammatory Syndrome in Children en-US
dc.type info:eu-repo/semantics/article
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